Neurodegeneration

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Neurodegeneration 

Neurodegeneration
Para-sagittal MRI of the head in a patient with benign familial macrocephaly

Neurodegeneration is the progressive loss of structure or function of neurons, which may ultimately involve cell death. Many neurodegenerative diseases—such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, and prion diseases—occur as a result of neurodegenerative processes. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable. Biomedical research has revealed many similarities between these diseases at the sub-cellular level, including atypical protein assemblies (like proteopathy) and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

Specific disorders

Alzheimer's disease

Comparison of brain tissue between healthy individual and Alzheimer's disease patient, demonstrating extent of neuronal death

Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the cerebral cortex and certain subcortical structures, resulting in gross atrophy of the temporal lobe, parietal lobe, and parts of the frontal cortex and cingulate gyrus. Even with billions of dollars being used to find a treatment for Alzheimer's disease, no effective treatments have been found. However, clinical trials have developed certain compounds that could potentially change the future of Alzheimer's disease treatments. Currently, diagnoses of Alzheimer's is subpar, and better methods need to be utilized for various aspects of clinical diagnoses. Alzheimer's has a 20% misdiagnosis rate.

AD pathology is primarily characterized by the presence of senile plaques and neurofibrillary tangles. Plaques are made up of small peptides, typically 39–43 amino acids in length, called beta-amyloid (also written as A-beta or Aβ). Beta-amyloid is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neuron's membrane. APP appears to play roles in normal neuron growth, survival and post-injury repair. APP is cleaved into smaller fragments by enzymes such as gamma secretase and beta secretase. One of these fragments gives rise to fibrils of beta-amyloid which can self-assemble into the dense extracellular deposits known as senile plaques or amyloid plaques.

Parkinson's disease

Parkinson's disease (PD) is the second most common neurodegenerative disorder. It typically manifests as bradykinesia, rigidity, resting tremor and posture instability. The crude prevalence rate of PD has been reported to range from 15 per 100,000 to 12,500 per 100,000, and the incidence of PD from 15 per 100,000 to 328 per 100,000, with the disease being less common in Asian countries.

PD is primarily characterized by death of dopaminergic neurons in the substantia nigra, a region of the midbrain. The cause of this selective cell death is unknown. Notably, alpha-synuclein-ubiquitin complexes and aggregates are observed to accumulate in Lewy bodies within affected neurons. It is thought that defects in protein transport machinery and regulation, such as RAB1, may play a role in this disease mechanism. Impaired axonal transport of alpha-synuclein may also lead to its accumulation in Lewy bodies. Experiments have revealed reduced transport rates of both wild-type and two familial Parkinson's disease-associated mutant alpha-synucleins through axons of cultured neurons. Membrane damage by alpha-synuclein could be another Parkinson's disease mechanism.

The main known risk factor is age. Mutations in genes such as α-synuclein (SNCA), leucine-rich repeat kinase 2 (LRRK2), glucocerebrosidase (GBA), and tau protein (MAPT) can also cause hereditary PD or increase PD risk. While PD is the second most common neurodegenerative disorder, problems with diagnoses still persist. Problems with the sense of smell is a widespread symptom of Parkinson’s disease (PD), however, some neurologists question its efficacy. This assessment method is a source of controversy among medical professionals. The gut microbiome might play a role in the diagnosis of PD, and research suggests various ways that could revolutionize the future of PD treatment.

Huntington's disease

Huntington's disease (HD) is a rare autosomal dominant neurodegenerative disorder caused by mutations in the huntingtin gene (HTT). HD is characterized by loss of medium spiny neurons and astrogliosis. The first brain region to be substantially affected is the striatum, followed by degeneration of the frontal and temporal cortices. The striatum's subthalamic nuclei send control signals to the globus pallidus, which initiates and modulates motion. The weaker signals from subthalamic nuclei thus cause reduced initiation and modulation of movement, resulting in the characteristic movements of the disorder, notably chorea. Huntington's disease presents itself later in life even though the proteins that cause the disease works towards manifestation from their early stages in the humans affected by the proteins. Along with being a neurodegenerative disorder, HD has links to problems with neurodevelopment.

HD is caused by polyglutamine tract expansion in the huntingtin gene, resulting in the mutant huntingtin. Aggregates of mutant huntingtin form as inclusion bodies in neurons, and may be directly toxic. Additionally, they may damage molecular motors and microtubules to interfere with normal axonal transport, leading to impaired transport of important cargoes such as BDNF. Huntington's disease currently has no effective treatments that would modify the disease.

Multiple sclerosis (MS)

Multiple sclerosis is a chronic debilitating demyelinating disease of the central nervous system, caused by an autoimmune attack resulting in the progressive loss of myelin sheath on neuronal axons.    The resultant decrease in the speed of signal transduction leads to a loss of functionality that includes both cognitive and motor impairment depending on the location of the lesion. The progression of MS occurs due to episodes of increasing inflammation, which is proposed to be due to the release of antigens such as myelin oligodendrocyte glycoprotein, myelin basic protein, and proteolipid protein, causing an autoimmune response. This sets off a cascade of signaling molecules that result in T cells, B cells, and Macrophages to cross the blood-brain barrier and attack myelin on neuronal axons leading to inflammation. Further release of antigens drives subsequent degeneration causing increased inflammation. Multiple sclerosis presents itself as a spectrum based on the degree of inflammation, a majority of patients suffer from early relapsing and remitting episodes of neuronal deterioration following a period of recovery. Some of these individuals may transition to a more linear progression of the disease, while about 15% of others begin with a progressive course on the onset of Multiple sclerosis. The inflammatory response contributes to the loss of the grey matter, and as a result current literature devotes itself to combatting the auto-inflammatory aspect of the disease. While there are several proposed causal links between EBV and the HLA-DRB1*15:01 allele to the onset of Multiple Sclerosis they may contribute to the degree of autoimmune attack and the resultant inflammation, they do not determine the onset of Multiple Sclerosis.

Amyotrophic lateral sclerosis (ALS)

Amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) is a disease in which motor neurons are selectively targeted for degeneration. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that negatively impacts the upper motor neurons (UMNs) and lower motor neurons (LMNs). In 1993, missense mutations in the gene encoding the antioxidant enzyme Cu/Zn superoxide dismutase 1 (SOD1) were discovered in a subsets of patients with familial ALS. This discovery led researchers to focus on unlocking the mechanisms for SOD1-mediated diseases. However, the pathogenic mechanism underlying SOD1 mutant toxicity has yet to be resolved. More recently, TDP-43 and FUS protein aggregates have been implicated in some cases of the disease, and a mutation in chromosome 9 (C9orf72) is thought to be the most common known cause of sporadic ALS. It is diagnosed by skeletal muscle weakness that progresses gradually. Early diagnosis of ALS is harder than with other neurodegenerative diseases as there are no highly effective means of determining its early onset. Currently, there is research being done regarding the diagnosis of ALS through upper motor neuron tests. The Penn Upper Motor Neuron Score (PUMNS) consists of 28 criteria with a score range of 0-32. A higher score indicates a higher level of burden present on the upper motor neurons. The PUMNS has proven quite effective in determining the burden that exists on upper motor neurons in affected patients.

Independent research provided in vitro evidence that the primary cellular sites where SOD1 mutations act are located on astrocytes. Astrocytes then cause the toxic effects on the motor neurons. The specific mechanism of toxicity still needs to be investigated, but the findings are significant because they implicate cells other than neuron cells in neurodegeneration.

Batten disease

Batten disease is a rare and fatal recessive neurodegenerative disorder that begins in childhood. Batten disease is the common name for a group of lysosomal storage disorders known as neuronal ceroid lipofuscinoses (NCLs) – each caused by a specific gene mutation, of which there are thirteen. Since Batten disease is quite rare, its worldwide prevalence is about 1 in every 100,000 live births. In North America, CLN3 disease (juvenile NCL) typically manifests between the ages of 4 to 7. Batten disease is characterized by motor impairment, epilepsy, dementia, vision loss, and shortened lifespan. A loss of vision is common first sign of Batten disease. Loss of vision is typically proceeded by cognitive and behavioral changes, seizures, and loss of the ability to walk. It is common for people to establish cardiac arrhythmias and difficulties eating food as the disease progresses. Batten disease diagnosis depends on a conflation of many criteria: clinical signs and symptoms, evaluations of the eye, electroencephalograms (EEG), and brain magnetic resonance imaging (MRI) results. The diagnosis provided by these results are corroborated by genetic and biochemical testing. No effective treatments were available to prevent the disease from being widespread before the past few years. In recent years, more models have been created to expedite the research process for methods to treat Batten disease.

Risk factor

The greatest risk factor for neurodegenerative diseases is aging. Mitochondrial DNA mutations as well as oxidative stress both contribute to aging. Many of these diseases are late-onset, meaning there is some factor that changes as a person ages for each disease. One constant factor is that in each disease, neurons gradually lose function as the disease progresses with age. It has been proposed that DNA damage accumulation provides the underlying causative link between aging and neurodegenerative disease. About 20-40% of healthy people between 60 and 78 years old experience discernable decrements in cognitive performance in several domains including working, spatial, and episodic memory, and processing speed.

Mechanisms

Genetics

Many neurodegenerative diseases are caused by genetic mutations, most of which are located in completely unrelated genes. In many of the different diseases, the mutated gene has a common feature: a repeat of the CAG nucleotide triplet. CAG codes for the amino acid glutamine. A repeat of CAG results in a polyglutamine (polyQ) tract. Diseases associated with such mutations are known as trinucleotide repeat disorders.

Polyglutamine repeats typically cause dominant pathogenesis. Extra glutamine residues can acquire toxic properties through a variety of ways, including irregular protein folding and degradation pathways, altered subcellular localization, and abnormal interactions with other cellular proteins. PolyQ studies often use a variety of animal models because there is such a clearly defined trigger – repeat expansion. Extensive research has been done using the models of nematode (C. elegans), and fruit fly (Drosophila), mice, and non-human primates.

Nine inherited neurodegenerative diseases are caused by the expansion of the CAG trinucleotide and polyQ tract, including Huntington's disease and the spinocerebellar ataxias.

Protein misfolding

Several neurodegenerative diseases are classified as proteopathies as they are associated with the aggregation of misfolded proteins. Protein toxicity is one of the key mechanisms of many neurodegenrative diseases.

• alpha-synuclein: can aggregate to form insoluble fibrils in pathological conditions characterized by Lewy bodies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Alpha-synuclein is the primary structural component of Lewy body fibrils. In addition, an alpha-synuclein fragment, known as the non-Abeta component (NAC), is found in amyloid plaques in Alzheimer's disease.
• tau: hyperphosphorylated tau protein is the main component of neurofibrillary tangles in Alzheimer's disease; tau fibrils are the main component of Pick bodies found in behavioral variant frontotemporal dementia.
• beta amyloid: the major component of senile plaques in Alzheimer's disease.
• prion: main component of prion diseases and transmissible spongiform encephalopathy.

Intracellular mechanisms

Protein degradation pathways

Parkinson's disease and Huntington's disease are both late-onset and associated with the accumulation of intracellular toxic proteins. Diseases caused by the aggregation of proteins are known as proteinopathies, and they are primarily caused by aggregates in the following structures:

• cytosol, e.g. Parkinson's & Huntington's
• nucleus, e.g. Spinocerebellar ataxia type 1 (SCA1)
• endoplasmic reticulum (ER), (as seen with neuroserpin mutations that cause familial encephalopathy with neuroserpin inclusion bodies)
• extracellularly excreted proteins, amyloid-β in Alzheimer's disease

There are two main avenues eukaryotic cells use to remove troublesome proteins or organelles:

• ubiquitin–proteasome: protein ubiquitin along with enzymes is key for the degradation of many proteins that cause proteinopathies including polyQ expansions and alpha-synucleins. Research indicates proteasome enzymes may not be able to correctly cleave these irregular proteins, which could possibly result in a more toxic species. This is the primary route cells use to degrade proteins.
  • Decreased proteasome activity is consistent with models in which intracellular protein aggregates form. It is still unknown whether or not these aggregates are a cause or a result of neurodegeneration.
• autophagy–lysosome pathways: a form of programmed cell death (PCD), this becomes the favorable route when a protein is aggregate-prone meaning it is a poor proteasome substrate. This can be split into two forms of autophagy: macroautophagy and chaperone-mediated autophagy (CMA).
  • macroautophagy is involved with nutrient recycling of macromolecules under conditions of starvation, certain apoptotic pathways, and if absent, leads to the formation of ubiquinated inclusions. Experiments in mice with neuronally confined macroautophagy-gene knockouts develop intraneuronal aggregates leading to neurodegeneration.
  • chaperone-mediated autophagy defects may also lead to neurodegeneration. Research has shown that mutant proteins bind to the CMA-pathway receptors on lysosomal membrane and in doing so block their own degradation as well as the degradation of other substrates.

Membrane damage

Damage to the membranes of organelles by monomeric or oligomeric proteins could also contribute to these diseases. Alpha-synuclein can damage membranes by inducing membrane curvature, and cause extensive tubulation and vesiculation when incubated with artificial phospholipid vesicles. The tubes formed from these lipid vesicles consist of both micellar as well as bilayer tubes. Extensive induction of membrane curvature is deleterious to the cell and would eventually lead to cell death.Apart from tubular structures, alpha-synuclein can also form lipoprotein nanoparticles similar to apolipoproteins.

Mitochondrial dysfunction

The most common form of cell death in neurodegeneration is through the intrinsic mitochondrial apoptotic pathway. This pathway controls the activation of caspase-9 by regulating the release of cytochrome c from the mitochondrial intermembrane space. Reactive oxygen species (ROS) are normal byproducts of mitochondrial respiratory chain activity. ROS concentration is mediated by mitochondrial antioxidants such as manganese superoxide dismutase (SOD2) and glutathione peroxidase. Over production of ROS (oxidative stress) is a central feature of all neurodegenerative disorders. In addition to the generation of ROS, mitochondria are also involved with life-sustaining functions including calcium homeostasis, PCD, mitochondrial fission and fusion, lipid concentration of the mitochondrial membranes, and the mitochondrial permeability transition. Mitochondrial disease leading to neurodegeneration is likely, at least on some level, to involve all of these functions.

There is strong evidence that mitochondrial dysfunction and oxidative stress play a causal role in neurodegenerative disease pathogenesis, including in four of the more well known diseases Alzheimer's, Parkinson's, Huntington's, and Amyotrophic lateral sclerosis.

Neurons are particularly vulnerable to oxidative damage due to their strong metabolic activity associated with high transcription levels, high oxygen consumption, and weak antioxidant defense.

DNA damage

The brain metabolizes as much as a fifth of consumed oxygen, and reactive oxygen species produced by oxidative metabolism are a major source of DNA damage in the brain. Damage to a cell’s DNA is particularly harmful because DNA is the blueprint for protein production and unlike other molecules it cannot simply be replaced by re-synthesis. The vulnerability of post-mitotic neurons to DNA damage (such as oxidative lesions or certain types of DNA strand breaks), coupled with a gradual decline in the activities of repair mechanisms, could lead to accumulation of DNA damage with age and contribute to brain aging and neurodegeneration. DNA single-strand breaks are common and are associated with the neurodegenerative disease ataxia-oculomotor apraxia. Increased oxidative DNA damage in the brain is associated with Alzheimer’s disease and Parkinson’s disease. Defective DNA repair has been linked to neurodegenerative disorders such as Alzheimer’s disease, amyotrophic lateral sclerosis, ataxia telangiectasia, Cockayne syndrome, Parkinson’s disease and xeroderma pigmentosum.

Axonal transport

Axonal swelling, and axonal spheroids have been observed in many different neurodegenerative diseases. This suggests that defective axons are not only present in diseased neurons, but also that they may cause certain pathological insult due to accumulation of organelles. Axonal transport can be disrupted by a variety of mechanisms including damage to: kinesin and cytoplasmic dynein, microtubules, cargoes, and mitochondria. When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered.

Programmed cell death

Programmed cell death (PCD) is death of a cell in any form, mediated by an intracellular program. This process can be activated in neurodegenerative diseases including Parkinson's disease, amytrophic lateral sclerosis, Alzheimer's disease and Huntington's disease. PCD observed in neurodegenerative diseases may be directly pathogenic; alternatively, PCD may occur in response to other injury or disease processes.

Apoptosis (type I)

Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death.

• Extrinsic apoptotic pathways: Occur when factors outside the cell activate cell surface death receptors (e.g., Fas) that result in the activation of caspases-8 or -10.
• Intrinsic apoptotic pathways: Result from mitochondrial release of cytochrome c or endoplasmic reticulum malfunctions, each leading to the activation of caspase-9. The nucleus and Golgi apparatus are other organelles that have damage sensors, which can lead the cells down apoptotic pathways.

Caspases (cysteine-aspartic acid proteases) cleave at very specific amino acid residues. There are two types of caspases: initiators and effectors. Initiator caspases cleave inactive forms of effector caspases. This activates the effectors that in turn cleave other proteins resulting in apoptotic initiation.

Autophagic (type II)

Autophagy is a form of intracellular phagocytosis in which a cell actively consumes damaged organelles or misfolded proteins by encapsulating them into an autophagosome, which fuses with a lysosome to destroy the contents of the autophagosome. Because many neurodegenerative diseases show unusual protein aggregates, it is hypothesized that defects in autophagy could be a common mechanism of neurodegeneration.

Cytoplasmic (type III)

PCD can also occur via non-apoptotic processes, also known as Type III or cytoplasmic cell death. For example, type III PCD might be caused by trophotoxicity, or hyperactivation of trophic factor receptors. Cytotoxins that induce PCD can cause necrosis at low concentrations, or aponecrosis (combination of apoptosis and necrosis) at higher concentrations. It is still unclear exactly what combination of apoptosis, non-apoptosis, and necrosis causes different kinds of aponecrosis.

Transglutaminase

Transglutaminases are human enzymes ubiquitously present in the human body and in the brain in particular.

The main function of transglutaminases is bind proteins and peptides intra- and intermolecularly, by a type of covalent bonds termed isopeptide bonds, in a reaction termed transamidation or crosslinking.

Transglutaminase binding of these proteins and peptides make them clump together. The resulting structures are turned extremely resistant to chemical and mechanical disruption.

Most relevant human neurodegenerative diseases share the property of having abnormal structures made up of proteins and peptides.

Each of these neurodegenerative diseases have one (or several) specific main protein or peptide. In Alzheimer's disease, these are amyloid-beta and tau. In Parkinson’s disease, it is alpha-synuclein. In Huntington’s disease, it is huntingtin.

Transglutaminase substrates: Amyloid-beta, tau, alpha-synuclein and huntingtin have been proved to be substrates of transglutaminases in vitro or in vivo, that is, they can be bonded by trasglutaminases by covalent bonds to each other and potentially to any other transglutaminase substrate in the brain.

Transglutaminase augmented expression: It has been proved that in these neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease) the expression of the transglutaminase enzyme is increased.

Presence of isopeptide bonds in these structures: The presence of isopeptide bonds (the result of the transglutaminase reaction) have been detected in the abnormal structures that are characteristic of these neurodegenerative diseases.

Co-localization: Co-localization of transglutaminase mediated isopeptide bonds with these abnormal structures has been detected in the autopsy of brains of patients with these diseases.

Management

The process of neurodegeneration is not well understood, so the diseases that stem from it have, as yet, no cures.

Animal models in research

In the search for effective treatments (as opposed to palliative care), investigators employ animal models of disease to test potential therapeutic agents. Model organisms provide an inexpensive and relatively quick means to perform two main functions: target identification and target validation. Together, these help show the value of any specific therapeutic strategies and drugs when attempting to ameliorate disease severity. An example is the drug Dimebon by Medivation, Inc. In 2009 this drug was in phase III clinical trials for use in Alzheimer's disease, and also phase II clinical trials for use in Huntington's disease. In March 2010, the results of a clinical trial phase III were released; the investigational Alzheimer's disease drug Dimebon failed in the pivotal CONNECTION trial of patients with mild-to-moderate disease. With CONCERT, the remaining Pfizer and Medivation Phase III trial for Dimebon (latrepirdine) in Alzheimer's disease failed in 2012, effectively ending the development in this indication.

In another experiment using a rat model of Alzheimer's disease, it was demonstrated that systemic administration of hypothalamic proline-rich peptide (PRP)-1 offers neuroprotective effects and can prevent neurodegeneration in hippocampus amyloid-beta 25–35. This suggests that there could be therapeutic value to PRP-1.

Other avenues of investigation

Protein degradation offers therapeutic options both in preventing the synthesis and degradation of irregular proteins. There is also interest in upregulating autophagy to help clear protein aggregates implicated in neurodegeneration. Both of these options involve very complex pathways that we are only beginning to understand.

The goal of immunotherapy is to enhance aspects of the immune system. Both active and passive vaccinations have been proposed for Alzheimer's disease and other conditions; however, more research must be done to prove safety and efficacy in humans.

A current therapeutic target for the treatment of Alzheimer's disease is the protease β-secretase^[, which is involved in the amyloidogenic processing pathway that leads to the pathological accumulation of proteins in the brain. When the gene that encodes for amyloid precursor protein (APP) is spliced by α-secretase rather than β-secretase, the toxic protein β amyloid is not produced. Targeted inhibition of β-secretase can potentially prevent the neuronal death that is responsible for the symptoms of Alzheimer's disease.

Self-compassion

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Self-compassion 

Self-compassion is extending compassion to one's self in instances of perceived inadequacy, failure, or general suffering. Kristin Neff has defined self-compassion as being composed of three main elements – self-kindness, common humanity, and mindfulness.

• Self-kindness: Self-compassion entails being warm towards oneself when encountering pain and personal shortcomings, rather than ignoring them or hurting oneself with self-criticism.
• Common humanity: Self-compassion also involves recognizing that suffering and personal failure is part of the shared human experience rather than isolating.
• Mindfulness: Self-compassion requires taking a balanced approach to one's negative emotions so that feelings are neither suppressed nor exaggerated. Negative thoughts and emotions are observed with openness, so that they are held in mindful awareness. Mindfulness is a non-judgmental, receptive mind state in which individuals observe their thoughts and feelings as they are, without trying to suppress or deny them. Conversely, mindfulness requires that one not be "over-identified" with mental or emotional phenomena, so that one suffers aversive reactions. This latter type of response involves narrowly focusing and ruminating on one's negative emotions.

Self-compassion in some ways resembles Carl Rogers' notion of "unconditional positive regard" applied both towards clients and oneself; Albert Ellis' "unconditional self-acceptance"; Maryhelen Snyder's notion of an "internal empathizer" that explored one's own experience with "curiosity and compassion"; Ann Weiser Cornell's notion of a gentle, allowing relationship with all parts of one's being; and Judith Jordan's concept of self-empathy, which implies acceptance, care and empathy towards the self.

Self-compassion is different from self-pity, a state of mind or emotional response of a person believing to be a victim and lacking the confidence and competence to cope with an adverse situation.

Research indicates that self-compassionate individuals experience greater psychological health than those who lack self-compassion. For example, self-compassion is positively associated with life satisfaction, wisdom, happiness, optimism, curiosity, learning goals, social connectedness, personal responsibility, and emotional resilience. At the same time, it is associated with a lower tendency for self-criticism, depression, anxiety, rumination, thought suppression, perfectionism, and disordered eating attitudes.

Self-compassion has different effects than self-esteem, a subjective emotional evaluation of the self. Although psychologists extolled the benefits of self-esteem for many years, recent research has exposed costs associated with the pursuit of high self-esteem, including narcissism, distorted self-perceptions, contingent and/or unstable self-worth, as well as anger and violence toward those who threaten the ego. As self-esteem is often associated with perceived self-worth in externalised domains such as appearance, academics and social approval, it is often unstable and susceptible to negative outcomes. In comparison, it appears that self-compassion offers the same mental health benefits as self-esteem, but with fewer of its drawbacks such as narcissism, ego-defensive anger, inaccurate self-perceptions, self-worth contingency, or social comparison.

Scales

Much of the research conducted on self-compassion so far has used the Self-Compassion Scale, created by Kristin Neff, which measures the degree to which individuals display self-kindness against self-judgment, common humanity versus isolation, and mindfulness versus over-identification.

The Self-Compassion Scale has been translated into different languages. Some of these include a Czech, Dutch, Japanese, Chinese, Turkish and Greek version.

Development

The original sample for which the scale was developed consisted of 68 undergraduate students from a large university in the United States. In this experiment, the participants narrowed down the potential scale items to 71.

The next stage of development involved testing the reliability and validity of the scale among a larger group of participants. During this research study, 391 undergraduate students were selected at random to complete the 71 previously narrowed down scale items. Based on their results, the number of items was reduced to 26. The self-compassion scales have good reliability and validity.

A second study was conducted to look more closely at the difference between self-esteem and self-compassion. This study consisted of 232 randomly selected, undergraduate students. Participants were asked to complete a number of different scales in questionnaire form. They were as follows: The 26-item Self-compassion Scale, the 10-item Rosenberg Self-esteem Scale, the 10-item Self-determination Scale, the 21-item Basic Psychological Needs Scale, and the 40-item Narcissistic Personality Inventory. Based on the findings, Neff reports "that self-compassion and self-esteem were measuring two different psychological phenomena."

A third study was conducted to examine the construct validity. By comparing two different groups of people, researchers would be able to see the different levels of self-compassion. Forty-three Buddhist practitioners completed the Self-compassion Scale as well as a self-esteem scale. The sample of 232 undergraduate students from the second study was used as the comparison group. As expected by Neff, the Buddhist practitioners had significantly higher self-compassion scores than the students.

Self-compassion scale

The long version of the Self-compassion scale (SCS) consists of 26 items. This includes 6 subscales – self-kindness, self-judgement, common humanity, isolation, mindfulness, and over-identification. Neff recommends this scale for ages 14 and up with a minimum 8th grade reading level.

Presented on a Likert scale, ranging from 1 (almost no self-compassion) to 5 (constant self-compassion), those completing the SCS are able to gain insight on how they respond to themselves during a struggle or challenging time.

Short form

The short version of the Self-Compassion Scale (SCS-SF) consists of 12 items and is available in Dutch and English. Research reveals that the short form scale can be used competently as a substitute for the long form scale. A study conducted at the University of Leuven, Belgium concluded that when examining total scores, this shorter version provides an almost perfect correlation with the longer version.

Six-factor model

Neff's scale proposes six interacting components of self-compassion, which can be grouped as three dimensions with two opposite facets. The first dimension is self-kindness versus self-judgment, and taps into how individuals emotionally relate to themselves. Self-kindness refers to one's ability to be kind and understanding of oneself, whereas self-judgement refers to being critical and harsh towards oneself. The second dimension is common humanity versus isolation, and taps into how people cognitively understand their relationship to others. Common humanity refers to one's ability to recognize that everyone is imperfect and that suffering is part of the human condition, whereas isolation refers to feeling all alone in one's suffering. The third dimension is mindfulness versus over-identification, and taps into how people pay attention to their pain. Mindfulness refers to one's awareness and acceptance of painful experiences in a balanced and non-judgmental way, whereas over-identification refers to being absorbed by and ruminating on one's pain. Neff argues the six components of self-compassion interact and operate as a system. Support for this view was demonstrated in a study which found that writing with either kindness, common humanity or mindfulness yielded increases on the other self-compassion dimensions.

Criticisms of Neff's scale

Currently, Kristin Neff's Self-Compassion Scale is the main self-report instrument used to measure self-compassion. Although it is widely accepted as being a reliable and valid tool to measure self-compassion, some researchers have posed questions regarding the scale's generalizability and its use of a six-factor model.

Generalizability

Although some have questioned the generalizability of Neff's Self-Compassion Scale, a recent study found support for the measurement invariance of the scale across 18 samples, including student, community, and clinical samples in 12 different translations.

Six-factor model

A 2015 study performed by Angélica López et al. examined the factor structure, reliability, and construct validity of the 24 item Dutch version of Neff's Self-compassion Scale using a large representative sample from the general population. The study consisted of 1,736 participants and used both a confirmatory factor analysis (CFA), and an exploratory factor analysis (EFA) to determine if Neff's six-factor structure could be replicated.

Lopez's study could not replicate the six-factor structure of Neff's Self-compassion Scale, but rather suggested a two-factor model of the scale, created by grouping the positive and negative items separately. Lopez argued that self-compassion and self-criticism are distinct.

More recently, however, a large 20 sample study (N=11,685) examined the factor structure of the SCS in 13 translations, using bifactor Exploratory Structural Equation Modeling, which is a more appropriate way to analyze constructs that operate as a system. In this comprehensive study one general factor and six specific factors had the best fit in every sample examined, while a two-factor solution had an inadequate fit. Moreover, over 95% of the reliable variance in item responding could be explained by a single general factor. This factor structure has been found to be invariant across cultures

Other evidence for the view that self-compassion is a global construct composed of six components that operate as a system stems from the fact that all six components change in tandem and are configured as a balanced system within individuals

Exercises

Self-compassion exercises generally consist of either a writing exercise, role-playing, or introspective contemplation, and are designed to foster self-kindness, mindfulness, and feelings of common humanity. Self-compassion exercises have been shown to be effective in increasing self-compassion, along with increases in self-efficacy, optimism, and mindfulness. These exercises have also been shown to decrease rumination. In individuals who were vulnerable to depression, one week of daily self-compassion exercises lead to reduced depression up to three months following the exercise, and increased happiness up to six months following the exercise, regardless of the pre-exercise levels of happiness.

How would you treat a friend?

This exercise asks the user to imagine that they are comforting a close friend who is going through a tough situation. The user is then asked to compare and contrast how they react internally to their own struggles, and to endeavour applying the same loving kindness to themselves that they would apply to a friend.

Self-compassion break

This exercise is to be used during times of acute distress. The user is asked to focus on a stressful event or situation. Then, the user is asked to repeat several prompts to themselves, each of which emphasizes one of the three main tenets of self-compassion: mindfulness, common humanity, and self-kindness.

Exploring through writing

In this exercise, the user is asked to focus on a facet of themself that they believe to be an imperfection, and that makes them feel inadequate. Once they have brought this issue to mind, they are asked to write a letter to themself from the perspective of an unconditionally loving imaginary friend. The user is then asked to focus on the soothing and comforting feelings of compassion that they have generated for themself.

Criticizer, criticized, and compassionate observer

This exercise asks the user to occupy several "chairs" during the course of the practice. Initially, they are asked to occupy the chair of the self-critic, and to express their feelings of self-criticism. They are asked to analyze this criticism and make note of its defining characteristics. Then, the user is asked to take the chair of their criticized self, and to imagine verbally responding to their inner critic. Subsequently, the user is prompted to conduct a dialogue between these two aspects of the self, the criticizer and the criticized. Following this, the user is asked to imagine themself as a compassionate observer of this dialogue, and finally the user is asked to reflect upon the experience.

Changing your critical self-talk

This exercise is meant to be conducted over several weeks, in the form of recurring reflection on the nature of their self-criticism. Users are asked to aim to notice when they are being self-critical, to react to their self-criticism with compassion, and to reframe the language of their inner critic.

Journal

This exercise entails keeping a daily journal for at least one week, and is used to reflect on difficult experiences, self-criticisms, and other stressors. The user is asked to analyze each of these events through the lenses of self-kindness (using gentle, comforting language to respond to the event), mindfulness (awareness of the negative emotions elicited by the situation), and common humanity (how the experience is part of the human condition).

Identifying what we really want

In this exercise, the user is asked to think about the ways that they use self-criticism as a way to motivate themself. Then, the user is asked to try to come up with a kinder and gentler and more caring way of motivating themself to make the desired change, and to try and be aware of how they use self-criticism as a motivational tool in the future.

Taking care of the caregiver

This exercise prompts the user to engage in meaningful self-care on a regular basis, and to practice these techniques while they are actively caring for others.

Self-forgiveness as an element

Self-forgiveness is an element of self-compassion that involves releasing self-directed negative feelings. Research has found that self-forgiveness promotes greater overall well-being, specifically higher self-esteem and lower neuroticism.

Pro-social behavior

When self-directed negative feelings are a result of negative past action, self-forgiveness does not mean ignoring or excusing offenses, but rather practicing self-compassion while taking full responsibility for past action. In this way, self-forgiveness may increase people's willingness to repent for wrongdoing. Despite this research, there is not yet a clear link between self-forgiveness and pro-social behavior. It would seem that accepting responsibility for negative actions leads to pro-social behavior, and coupling acceptance with self-forgiveness increases this effect.

Self-acceptance as an element

Self-acceptance is an element of self-compassion that involves accepting oneself for who and what they are. Self-acceptance differs from self-esteem in that self-esteem involves globally evaluating one's worth. Self-acceptance means accepting the self despite flaws, weaknesses, and negative evaluations from others.

Mindfulness

History

The concept of mindfulness and self-compassion has been around for over 2500 years, and is rooted in Eastern traditional Buddhist philosophy and Buddhist meditation. In Buddhist philosophy, mindfulness and compassion is considered to be two wings of one bird, with each concept overlapping one another but producing benefits for wellbeing. The word Mindfulness is the English translation of the word Vipassan, which a combination of two words Vi, meaning in a special way and Passana, to observe, hence implying to observe in a special way. Compassion (karunaa) can be defined as an emotion that elicits the wanting to be free from suffering. Mindfulness in the context of self-compassion comprises acknowledging one's painful experiences in a balanced way that neither ignores, or ruminates on the disliked characteristics of oneself or life. According to Neff (2012) it is essential to be mindful of one's own personal suffering in order to extend compassion towards one's self. However it is essential to pay attention to self suffering in a grounded way in order to avoid "over-identification". Mindfulness tends to focus on the internal experience such as sensation, emotion and thoughts rather than focusing on the experiencer. Self-compassion focuses on soothing and comforting the self when faced with distressing experiences. Self-compassion is composed of three components; self kindness versus self-judgement, a sense of common humanity versus isolation and mindfulness versus over-identification when confronting painful thoughts and emotions.

Mindfulness-based stress reduction

Mindfulness-based stress reduction (MBSR), developed by Jon Kabat-Zinn is a structured group program that uses mindfulness meditation to relieve suffering associated with physical, psychosomatic and psychiatric disorders. Mindfulness-based stress reduction therapy seeks to increase the capacity for mindfulness, by reducing the need for self-focused thoughts and emotions that can lead to poor mental health. The exercise of mindfulness-based stress reduction therapy brings together the elements of meditation and yoga, greater awareness of the unity of mind and body, as well as the ways that the unconscious thoughts, feelings, and behaviors can undermine emotional, physical, and spiritual health. Clinical research from the past 25 years has found that MBSR is efficacious in reducing distress and enhancing individual well-being. Self-Compassion can play a critical role in mindfulness-based cognitive therapy interventions.the study Shapiro et al. (2005) found that health care professionals who underwent a MBSR program reported significantly increased self-compassion and reduced stress levels compared to the waitlist control group. It was also reported that the increase of self-compassion appeared to reduce stress associated with the program.

Mindfulness-based cognitive therapy

Mindfulness-based cognitive therapy (MBCT) is an intervention therapy that combines meditation practices, psycho-education and cognitive behavioral strategies to prevent the relapse or recurrence of major depression. MBCT teaches individuals how to observe their thoughts and feelings by focusing their attention on natural objects, such as breathing and bodily sensations. Individuals are taught how to achieve awareness while holding an attitude of non-judgemental acceptance. Within MBCT, mindfulness skills are taught in order to recognize distressing thoughts and feelings, to be aware of these experiences, and utilize acceptance and self-compassion to break up associative networks that may cause a relapse. Self-compassion in response to negative thoughts and feelings is an adaptive process, which validates it as a key learning skill in MBCT. Self-compassion has been found to be a key mechanism in the effectiveness of mindfulness-based interventions such as mindfulness-based cognitive therapy (MBCT). Kuyken et al. (2010) compared the effect of MBCT with maintenance antidepressants on relapse in depressive symptoms. They found that mindfulness and self-compassion were increased after MBCT was introduced. They also found that MBCT reduced the connection of cognitive reactivity and depressive relapse, and that the increased self-compassion helped mediate this association.

Mindfulness-based pain management

Mindfulness-based pain management (MBPM) is a mindfulness-based intervention (MBI) providing specific applications for people living with chronic pain and illness. Adapting the core concepts and practices of mindfulness-based stress reduction (MBSR) and mindfulness-based cognitive therapy (MBCT), MBPM includes a distinctive emphasis on the practice of 'loving-kindness', and has been seen as sensitive to concerns about removing mindfulness teaching from its original ethical framework within Buddhism. It was developed by Vidyamala Burch and is delivered through the programs of Breathworks. It has been subject to a range of clinical studies demonstrating its effectiveness.

Mindful self-compassion therapy

Mindful self-compassion (MSC) therapy is a hybrid therapy consisting of self-compassion and mindfulness practices. The term mindful is referred to in the MSC program as the basic mindfulness skills which is turning toward painful thoughts and emotions and seeing them as they are without suppression or avoidance which is crucial to the development of self-compassion. The MSC program however focuses more on self-compassion and sees mindfulness as a secondary emphasis. MSC teaches both formal (meditation) and informal (daily life) self-compassion practices. In addition there are homework MSC assignments that teaches participants to be kinder to themselves. The goal of MSC therapy is to provide participants with a variety of tools to increase self-compassion which they can then in turn integrate into their lives. A study conducted by Neff and Germer (2012) found that compared with the control group, MSC intervention participants reported significantly larger increases in self-compassion, mindfulness, wellbeing and a decrease in depression, stress and anxiety which were maintained for 6 months after the initial intervention.

Compassion focused therapy

Paul Gilbert (2009) developed compassion focused therapy (CFT) that teaches clients that, due to how our brains have evolved, anxiety, anger and depression are natural experiences that are occur through no fault of our own. Patients are trained to change maladaptive thought patterns such as "I'm unlovable" and provide alternative self-statements, such as "know for sure that some people love me". The goal of CFT is to help patients develop a sense of warmth and emotional responsiveness to oneself. This is achieved through a variety of exercises including visualization, cultivating self-kindest through language by engaging in self-compassionate behaviors and habits. In CFT self-compassion is utilized through thoughts, images, and attention which is needed to stimulate and develop the contentment, sooth and safeness system.

Mindfulness skills in dialectical behavior therapy

Dialectical behavior therapy (DBT), is a derivative of cognitive behavior therapy that incorporates Eastern meditative practice. DBT is based on a dialectical world view that incorporates the balance and integration of opposing beliefs, particularly in acceptance and change. We accept ourselves as good enough, and we recognize the need for all of us to change and grow. Unlike MBCT and MBSR therapies, dialectical behavior therapy does not use meditation but less formal exercises, such as individual therapy sessions and group skill sessions. In general last for approximately a year where participants will engage in weekly individual skill therapy sessions and group skill sessions. The skills therapy sessions include four segments; core mindfulness, interpersonal effectiveness, emotion regulation, and distress tolerance skills. Dialectical behaviour therapist recommend developing self-compassion. The basic premise of using self-compassion therapies in DBT is to cultivate a compassionate mind state, defined by feelings of warmth, safety, presence and interconnectedness that can in turn relieve emotional dysregulation.

Mindfulness and related skills in acceptance and commitment therapy

Acceptance and commitment therapy utilizes behavior change process, mindfulness and acceptance process. ACT, involves non-judgmental awareness and openness to cognitive sensation an emotional experiences. It also promotes exposure to previously avoided situations that have caused anxiety in order to promote acceptance. The avoidant behavior is treated by having clients observing their thoughts and accepting that their thoughts are not necessarily harmful. In general ACT strategies are customized to fit each participant so they obtain psycho-education, problem solving skills and psychological flexibility. Mindfulness and acceptance exercises and skills facilitate the behavioral changes necessary for its user to pursue a life that they feel is vital and meaningful. Various sources have indicated that acceptance and commitment therapy overlaps with Neff's conceptualization of self compassion particularly ACT's relational frame theory. The basic theories and concepts underlining ACT, may be relevant and have shown to be parallels and hold similarities found in self-compassion The first is ACT's perspective and Neff's concept of self-kindness are both linked to self-acceptance. Acceptance of one's painful experiences and hurt is related to kindness to one's self. Second Neff's conceptualization of self-compassion and ACT both emphasize mindfulness, which is practiced in ACT through the concepts of defusion, acceptance, contact with the present moment and the self as a context. Defusion is also used in self-compassion as a means of allowing self-criticisms to pass through the mind without believing, proving them wrong or engaging in a stance to make these thoughts workable. In a study conducted by Yadavaia, Hayes & Vilardaga, 2014 test the efficacy of an ACT approach to self-compassion as compared to a waitlist control, the study showed that ACT interventions led to a large increase in self-compassion and psychopathology compared to the waitlist control at post-treatment and two months post intervention.

 

Self

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Self

The self is an individual person as the object of its own reflective consciousness. Since the self is a reference by a subject to the same subject, this reference is necessarily subjective. The sense of having a self—or self-hood—should, however, not be confused with subjectivity itself. Ostensibly, this sense is directed outward from the subject to refer inward, back to its "self" (or itself). Examples of psychiatric conditions where such "sameness" may become broken include depersonalization, which sometimes occurs in schizophrenia: the self appears different from the subject.

The first-person perspective distinguishes self-hood from personal identity. Whereas "identity" is (literally) sameness and may involve categorization and labeling, self-hood implies a first-person perspective and suggests potential uniqueness. Conversely, we use "person" as a third-person reference. Personal identity can be impaired in late-stage Alzheimer's disease and in other neurodegenerative diseases. Finally, the self is distinguishable from "others". Including the distinction between sameness and otherness, the self versus other is a research topic in contemporary philosophy and contemporary phenomenology, psychology, psychiatry, neurology, and neuroscience.

Although subjective experience is central to self-hood, the privacy of this experience is only one of many problems in the Philosophy of self and scientific study of consciousness.

Neuroscience

Two areas of the brain that are important in retrieving self-knowledge are the medial prefrontal cortex and the medial posterior parietal cortex. The posterior cingulate cortex, the anterior cingulate cortex, and medial prefrontal cortex are thought to combine to provide humans with the ability to self-reflect. The insular cortex is also thought to be involved in the process of self-reference.

Psychology

The psychology of self is the study of either the cognitive and affective representation of one's identity or the subject of experience. The earliest formulation of the self in modern psychology forms the distinction between the self as I, the subjective knower, and the self as Me, the subject that is known. Current views of the self in psychology position the self as playing an integral part in human motivation, cognition, affect, and social identity. Self following from John Locke has been seen as a product of episodic memory but research upon those with amnesia find they have a coherent sense of self based upon preserved conceptual autobiographical knowledge. It is increasingly possible to correlate cognitive and affective experience of self with neural processes. A goal of this ongoing research is to provide grounding and insight into the elements of which the complex multiply situated selves of human identity are composed. The 'Disorders of the Self' have also been extensively studied by psychiatrists.

For example, facial and pattern recognition take large amounts of brain processing capacity but pareidolia cannot explain many constructs of self for cases of disorder, such as schizophrenia or schizo-affective disorder. One's sense of self can also be changed upon becoming part of a stigmatized group. According to Cox, Abramson, Devine, and Hollon (2012), if an individual has prejudice against a certain group, like the elderly and then later becomes part of this group this prejudice can be turned inward causing depression (i.e. deprejudice).

The philosophy of a disordered self, such as in schizophrenia, is described in terms of what the psychiatrist understands are actual events in terms of neuron excitation but are delusions nonetheless, and the schizo-affective or schizophrenic person also believes are actual events in terms of essential being. PET scans have shown that auditory stimulation is processed in certain areas of the brain, and imagined similar events are processed in adjacent areas, but hallucinations are processed in the same areas as actual stimulation. In such cases, external influences may be the source of consciousness and the person may or may not be responsible for "sharing" in the mind's process, or the events which occur, such as visions and auditory stimuli, may persist and be repeated often over hours, days, months or years—and the afflicted person may believe themselves to be in a state of rapture or possession.

What the Freudian tradition has subjectively called, "sense of self" is for Jungian analytic psychology, where one's identity is lodged in the persona or ego and is subject to change in maturation. Carl Jung distinguished, "The self is not only the center, but also the whole circumference which embraces both conscious and unconscious; it is the center of this totality...". The Self in Jungian psychology is "the archetype of wholeness and the regulating center of the psyche ... a transpersonal power that transcends the ego." As a Jungian archetype, it cannot be seen directly, but by ongoing individuating maturation and analytic observation, can be experienced objectively by its cohesive wholeness making factor.

Meanwhile self psychology is a set of psychotherapeutic principles and techniques established by the Austrian-born American psychoanalyst Heinz Kohut upon the foundation of the psychoanalytic method developed by Freud, and is specifically focused on the subjectivity of experience, which it alleges is mediated by a psychological structure called the self.

Sociology

The self can be redefined as a dynamic, responsive process that structures neural pathways according to past and present environments including material, social, and spiritual aspects. Self-concept is a concept or belief that an individual has of him or herself as an emotional, spiritual, and social being. Therefore, the self-concept is the idea of who I am, kind of like a self-reflection of one's well-being. For example, the self-concept is anything you say about yourself.

A society is a group of people who share a common belief or aspect of self interacting for the maintenance or betterment of the collective. Culture consists of explicit and implicit patterns of historically derived and selected ideas and their embodiment in institutions, cognitive and social practices, and artifacts. Cultural systems may, on the one hand, be considered as products of action, and on the other, as conditioning elements of further action. Therefore, the following sections will explore how the self and self-concept can be changed due to different cultures.

Markus and Kitayama's early 1990s theory hypothesized that representations of the self in human cultures would fall on a continuum from independent to interdependent. The independent self is supposed to be egoistic, unique, separated from the various contexts, critical in judgement and prone to self-expression. The interdependent self is supposed to be altruistic, similar with the others, flexible according to contexts, conformist and unlikely to express opinions that would disturb the harmony of his or her group of belonging. This theory enjoyed huge popularity despite its many problems such as being based on popular stereotypes and myths about different cultures rather than on rigorous scientific research as well as postulating a series of causal links between culture and self-construals without presenting any evidence supporting them. A large study from 2016 involving a total of 10,203 participants from 55 cultural groups found that there is no independent versus interdependent dimension of self-construal because traits supposed by Markus & Kitayama to form a coherent construct do not actually correlate, or if they correlate, they have correlations opposite to those postulated by Markus & Kitayama. There are seven separate dimension of self-construal which can be found at both the cultural level of analysis and the individual level of analysis. These dimensions are difference versus similarity (if the individual considers himself or herself to be a unique person or to be the same as everybody else), self-containment versus connection to others (feeling oneself as being separated from others versus feeling oneself as being together with the others), self-direction versus receptiveness to influence (independent thinking versus conformity),

Westerners, Latin Americans and the Japanese are relatively likely to represent their individual self as unique and different from that of others while Arabs, South-East Asians and Africans are relatively likely to represent their self as being similar with that of others. Individuals from Uganda, Japan, Colombia, Namibia, Ghana and Belgium were most likely to represent their selves as being emotionally separated from the community while individuals from Oman, Malaysia, Thailand and central Brazil were most likely to consider themselves as emotionally connected to their communities. Japanese, Belgians, British and Americans from Colorado were most likely to value independent thinking and consider themselves as making their own decisions in life independently from others. On the other hand, respondents from rural Peru, Malaysia, Ghana, Oman and Hungary were most likely to place more value on following others rather than thinking for themselves as well as to describe themselves as being often influenced by others in their decisions. Middle Easterners from Lebanon, Turkey, Egypt and Oman were most likely to value self-reliance and consider themselves as working on their own and being economically independent from others. On the other hand, respondents from Uganda, Japan and Namibia were most likely to consider cooperation between different individuals in economical activities as being important. Chileans, Ethiopians from the highlands, Turks and people from Lebanon placed a relatively high degree of importance on maintaining a stable pattern of behavior regardless of situation or context. Individuals from Japan, Cameroon, the United Kingdom and Sweden were most likely to describe themselves as being adaptable to various contexts and to place value on this ability. Colombians, Chileans, US Hispanics, Belgians and Germans were most likely to consider self expression as being more important than maintaining harmony within a group. Respondents from Oman, Cameroon and Malaysia were most likely to say that they prefer keeping harmony within a group to engaging in self-expression. Sub-Saharan Africans from Namibia, Ghana and Uganda considered that they would follow their own interests even if this means harming the interests of those close to them. Europeans from Belgium, Italy and Sweden had the opposite preference, considering self-sacrifice for other members of the community as being more important than accomplishing selfish goals.

Contrary to the theory of Markus & Kitayama, egoism correlates negatively with individual uniqueness, independent thinking and self-expression. Self-reliance correlates strongly and negatively with emotional self-containment, which is also unexpected given Markus & Kitayama's theory. The binary classification of cultural self-construals into independent versus interdependent is deeply flawed because in reality, the traits do not correlate according to Markus & Kitayama's self construal theory, and this theory fails to take into consideration the extremely diverse and complex variety of self-construals present in various cultures across the world.

The way individuals construct themselves may be different due to their culture. The self is dynamic and complex and it will change or conform to whatever social influence it is exposed to. The main reason why the self is constantly dynamic is because it always looks for reasons to not be harmed. The self in any culture looks out for its well-being and will avoid as much threat as possible. This can be explained through the evolutionary psychology concept called survival of the fittest.

Philosophy

The philosophy of self seeks to describe essential qualities that constitute a person's uniqueness or essential being. There have been various approaches to defining these qualities. The self can be considered that being which is the source of consciousness, the agent responsible for an individual's thoughts and actions, or the substantial nature of a person which endures and unifies consciousness over time.

In addition to Emmanuel Levinas writings on "otherness", the distinction between "you" and "me" has been further elaborated in Martin Buber's philosophical work: Ich und Du.

Religion

Religious views on the self vary widely. The self is a complex and core subject in many forms of spirituality. Two types of self are commonly considered—the self that is the ego, also called the learned, superficial self of mind and body, an egoic creation, and the self which is sometimes called the "True Self", the "Observing Self", or the "Witness". In Hinduism, the Ātman (self), despite being experienced as individual, is actually a representation of the unified transcendent reality, Brahman. Our experience of reality doesn't match the nature of Brahman due to māyā.

One description of spirituality is the self's search for "ultimate meaning" through an independent comprehension of the sacred. Another definition of spiritual identity is: "A persistent sense of self that addresses ultimate questions about the nature, purpose, and meaning of life, resulting in behaviors that are consonant with the individual’s core values. Spiritual identity appears when the symbolic religious and spiritual value of a culture is found by individuals in the setting of their own life. There can be different types of spiritual self because it is determined by one's life and experiences."

Human beings have a self—that is, they are able to look back on themselves as both subjects and objects in the universe. Ultimately, this brings questions about who we are and the nature of our own importance. Traditions such as Buddhism see the attachment to self is an illusion that serves as the main cause of suffering and unhappiness. Christianity makes a distinction between the true self and the false self, and sees the false self negatively, distorted through sin: 'The heart is deceitful above all things, and desperately wicked; who can know it?' (Jeremiah 17:9)

According to Marcia Cavell, identity comes from both political and religious views. He also identified exploration and commitment as interactive parts of identity formation, which includes religious identity. Erik Erikson compared faith with doubt and found that healthy adults take heed to their spiritual side.